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Epstein-Barr virus-driven lymphomagenesis in the context of human immunodeficiency virus type 1 infection

Overview of attention for article published in Frontiers in Microbiology, January 2013
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Title
Epstein-Barr virus-driven lymphomagenesis in the context of human immunodeficiency virus type 1 infection
Published in
Frontiers in Microbiology, January 2013
DOI 10.3389/fmicb.2013.00311
Pubmed ID
Authors

Maria R. Petrara, Riccardo Freguja, Ketty Gianesin, Marisa Zanchetta, Anita De Rossi

Abstract

Epstein-Barr virus (EBV) is a ubiquitous human γ-herpes virus which establishes a life-long asymptomatic infection in immunocompetent hosts. In human immunodeficiency virus type 1 (HIV-1) infected patients, the impaired immunosurveillance against EBV may favor the development of EBV-related diseases, ranging from lymphoproliferative disorders to B cell non-Hodgkin's lymphomas (NHL). Antiretroviral therapy (ART) has significantly modified the natural course of HIV-1 infection, resulting in decreased HIV-1 plasmaviremia, increased CD4 lymphocytes, and decreased opportunistic infections, indicating a restoration of immune functions. However, the impact of ART appears to be less favorable on EBV-related malignancies than on other AIDS-defining tumors, such as Kaposi's sarcoma, and NHL remains the most common cancer during the ART era. EBV-driven tumors are associated with selective expression of latent oncogenic proteins, but uncontrolled lytic cycle with virus replication and/or reactivation may favor cell transformation, at least in the early phases. Several host's factors may promote EBV reactivation and replication; besides immunodepression, inflammation/chronic immune stimulation may play an important role. Microbial pathogen-associated molecular patterns and endogenous damage-associated molecular patterns, through Toll-like receptors, activate the immune system and may promote EBV reactivation and/or polyclonal expansion of EBV-infected cells. A body of evidence suggests that chronic immune stimulation is a hallmark of HIV-1 pathogenesis and may persist even in ART-treated patients. This review focuses on lymphomagenesis driven by EBV both in the context of the natural history of HIV-1 infection and in ART-treated patients. Understanding the mechanisms involved in the expansion of EBV-infected cells is a premise for the identification of prognostic markers of EBV-associated malignancies.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 50 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 50 100%

Demographic breakdown

Readers by professional status Count As %
Student > Master 9 18%
Researcher 6 12%
Student > Ph. D. Student 6 12%
Unspecified 5 10%
Student > Bachelor 4 8%
Other 10 20%
Unknown 10 20%
Readers by discipline Count As %
Medicine and Dentistry 12 24%
Agricultural and Biological Sciences 11 22%
Biochemistry, Genetics and Molecular Biology 6 12%
Unspecified 5 10%
Immunology and Microbiology 4 8%
Other 2 4%
Unknown 10 20%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 18 October 2013.
All research outputs
#20,207,295
of 22,727,570 outputs
Outputs from Frontiers in Microbiology
#22,173
of 24,581 outputs
Outputs of similar age
#248,792
of 280,760 outputs
Outputs of similar age from Frontiers in Microbiology
#264
of 407 outputs
Altmetric has tracked 22,727,570 research outputs across all sources so far. This one is in the 1st percentile – i.e., 1% of other outputs scored the same or lower than it.
So far Altmetric has tracked 24,581 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 6.3. This one is in the 1st percentile – i.e., 1% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 280,760 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 1st percentile – i.e., 1% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 407 others from the same source and published within six weeks on either side of this one. This one is in the 1st percentile – i.e., 1% of its contemporaries scored the same or lower than it.